Links for Keyword: Parkinsons
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CHICAGO – Deep brain stimulation of two different areas of the brain appears to improve problems with uncontrolled movements (dyskinesia) in patients with Parkinson disease (PD), according to an article in the April issue of Archives of Neurology, one of the JAMA/Archives journals. Deep brain stimulation with electrical impulses delivered to structures deep within the brain is being intensively investigated for the management of advanced Parkinson disease, according to background information in the article. Although a number of studies have shown that stimulation of two different areas of the brain, the globus pallidus interna (GPi) and the subthalmic nucleus (STN), can be achieved safely and effectively, STN has been thought to be the preferred target. At the same time, the authors note, there does seem to be some evidence that the STN is more vulnerable during surgery and that STN patients may have more postoperative problems. Valerie C. Anderson, Ph.D., of the Oregon Health and Science University, Portland, and colleagues compared 23 patients with Parkinson disease and problems with medication-induced uncontrolled movement who were randomly assigned to implantation of deep brain stimulators in either the GPi or the STN areas of the brain. Patients' Parkinson symptoms were evaluated with and without medication using a standard rating scale at three, six and 12 months after surgery.
INDIANAPOLIS – A mutation in a recently discovered Parkinson's disease gene is believed to be the most common genetic cause of inherited forms of the disease, according to a Parkinson Study Group study appearing in The Lancet in January. Researchers say the mutation on the LRRK2 gene is responsible for 5 percent of inherited Parkinson's disease cases. Tatiana Foroud, Ph.D., associate professor of medical and molecular genetics at Indiana University School of Medicine and principal investigator on the multi-site study, said the discovery has a broad implication for genetic screening for the disease. "Our results suggest that the mutation we have studied is the most common cause of Parkinson's disease identified to date," said Dr. Foroud. "While a great deal of work remains to be done, it is clear that any future genetic testing for Parkinson's disease must include studies of the LRRK2 gene." The patients in the Indiana University study who had the mutation had longer disease duration but less severe symptoms when they were participating in the trial. That suggests that the mutation may be associated with slower disease progression, said Dr. Foroud.
PORTLAND, Ore. – A peculiar form of a gene mutation known to increase a person's risk for Parkinson's disease is puzzling doctors about how to counsel patients who have the anomaly. A study by researchers at the Oregon Health & Science University School of Medicine's Parkinson Center of Oregon, the University of Washington School of Medicine and the New York State Department of Health, Wadsworth Center, raises concerns about whether patients testing positive for a single mutation of the parkin gene, rather than the two mutations typically required for developing Parkinson's, can be accurately informed about their risks of developing the disease or passing it on to their children. The study represents "a call for getting more information about the gene," said John "Jay" G. Nutt, M.D., OHSU professor of neurology, and physiology and pharmacology, and Parkinson center director. "What are the clinical implications of finding this gene?" What's alarmed doctors is that in the clinical setting, the single mutation appears to be common: 18 percent of patients with early-onset Parkinson's disease – those diagnosed before age 40 – tested positive for parkin gene mutations, and of that group, 70 percent had only one mutation.
But antidepressant Paxil has no effect on physical symptoms PORTLAND, Ore. – A well-known drug used to treat hyperactive children boosts the potency of another drug that reduces Parkinson's disease symptoms, an Oregon Health & Science University study has found. Scientists at the OHSU Parkinson Center of Oregon found that methylphenidate, known commercially as Ritalin, bolsters the effects of levodopa, a drug converted in the brain to dopamine. Methylphenidate inhibits the reabsorption of dopamine into nerve cells, increasing the neurotransmitter's potency. Parkinson's disease is caused by a deficiency of nerve cells that produce dopamine. A parallel study by Parkinson center researchers found that paroxetine, a popular antidepressant best known under the brand name Paxil, doesn't augment the effects of levodopa and has little benefit in reducing physical symptoms of Parkinson's disease.
ST. PAUL, MN – People with high levels of iron in their diet are more likely to develop Parkinson's disease, according to a study in the June 10 issue of Neurology, the scientific journal of the American Academy of Neurology. People with both high levels of iron and manganese were nearly two times more likely to develop the disease than those with the lowest levels of the minerals in their diets. The study compared 250 people who were newly diagnosed with Parkinson's to 388 people without the disease. Interviews were conducted to determine how often participants ate certain foods during their adult life. Those who had the highest level of iron in their diets – in the top 25 percent – were 1.7 times more likely to be Parkinson's patients than those in the lowest 25 percent of iron intake. Those whose level of both iron and manganese was higher than average were 1.9 times more likely to be Parkinson's patients than those with lower than average intake of the minerals.
Findings suggest how tiny jolts can steady tremor sufferers By ALEXANDRA WITZE / The Dallas Morning News ORLANDO, Fla. – Everybody likes to stimulate their brains, usually to make themselves feel smarter. But for some people, it's a medical necessity. People who suffer from Parkinson's or other tremor-related diseases sometimes benefit from deep brain stimulation – a surgery in which doctors implant a small device that sends an electrical signal to a specific part of the brain. Just as a pacemaker uses electricity to regulate an erratic heartbeat, deep brain stimulation uses electricity to pace the firing of nerve cells, or neurons, that control movement. Used with or instead of medication, the surgery often lets patients regain control over involuntary jerks like those experienced during Parkinson's. But nobody knows why. ©2002 Belo Interactive
First-ever clinical trials using gene therapy for Parkinson's disease anticipated to begin by end of year – Auckland, New Zealand and New York, NY: In a study published today in the journal Science, scientists from the University of Auckland and Weill Cornell Medical College reported on the effectiveness of a new gene therapy approach to Parkinson's Disease, and the potential for this therapy to affect the overall progression of the disease itself. Based on this study and other data, the U.S. Food and Drug Administration (FDA) has given its approval to begin testing this therapy in a small Phase I clinical trial. This will be the first time in the world that gene therapy will be used in patients with Parkinson's Disease. The Science publication is authored by lead investigator, Dr. Matthew J. During, Professor of Molecular Medicine at the University of Auckland, first author Dr. Jia Luo, and co-investigator Dr. Michael G. Kaplitt, Director of Stereotactic and Functional Neurosurgery and Asst. Professor at Weill Cornell Medical College. Dr. During and Dr. Kaplitt are also co-principal investigators on the upcoming clinical trial of this therapy. "We are using gene therapy to "re-set" a specific group of cells that have become overactive in an affected part of the brain, causing the impaired movement and other symptoms associated with Parkinson's Disease," said Dr. During. "We are very encouraged that in addition to the affect this therapy has on quieting symptoms, we present evidence that suggests it may arrest or delay disease progression."
GAINESVILLE, Fla.---Scientists report this week they have demonstrated that the injection of two corrective genes into a specific brain region generated significant restoration of normal limb movement in rats with a chemical-induced form of Parkinson’s disease. The findings – by a team of researchers from the University of Florida in Gainesville and Lund University in Lund, Sweden – are published in the current online version of the journal of the Proceedings of the National Academy of Sciences. Neuroscientists Anders Bjorklund of Sweden and Ronald Mandel with UF said the strategy that proved effective in the rodents is not a cure for Parkinson’s disease, but is expected to lead to a better method for delaying and controlling symptoms of the progressively disabling condition. About 1 million Americans are affected by Parkinson’s disease, which occurs most often between the ages of 65 and 90. "We found that the simultaneous delivery of two selected genes, coupled with a powerful gene-activating agent, works like a pump to prime the production of L-dopa, which is then converted into dopamine by appropriate nerve cells in the brain," said Mandel, a professor of neuroscience with UF’s Evelyn F. and William L. McKnight Brain Institute and the UF Genetics Institute. Dopamine is a neurotransmitter chemical that plays a lead role in coordinating limb movements.
NASHVILLE, Tenn., – It was a warm summer night that Tuesday – a night not unlike many others he had spent working in the lab – when Richard Nass, Ph.D. walked down the empty hallway and entered a small, darkened room. Settling himself onto a stool, he placed a shallow dish on the stage of the microscope before him and peered through the eyepieces. What he saw there – or, rather, didn’t see – took him aback. Nass saw the host of wriggling, transparent worms that he expected, but missing was the distinctive green glow that should have lit up the bodies of the worms like neon. "I almost couldn’t believe it," he said, shaking his head. The loss of green fluorescence that Nass observed in his worms told him that their dopamine neurons, which had been genetically altered to fluoresce green, had been destroyed by exposure to a chemical, 6-hydroxydopamine (6-OHDA). The results of the study, published this week in the journal Proceedings of the National Academy of Sciences, suggest that this tiny roundworm, named C.elegans, can serve as a powerful model for studying the molecular mechanisms underlying degeneration of dopamine neurons in the brains of patients with Parkinson’s disease (PD).
By Alison McCook Over the course of 5 days last summer, an army of researchers and clinicians examined, poked, and prodded 1-year-old Hannah Ostrea at the National Institutes of Health (NIH). Experts in neurology, rehabilitation medicine, physical therapy, speech pathology, and anesthesiology gave the little girl an EEG, a test of her heart’s electrical activity (EKG), an MRI, a CT scan, X-rays, and a throat exam (laryngoscopy). All this testing was meant not only to help Hannah but in the hope that her rare disease could reveal something about another condition that affects 1 million Americans: Parkinson’s. Hannah has Gaucher’s disease, and within hours of her birth, it was obvious something was wrong. Looking past her thick head of dark hair, and the fact that she could down an entire bottle of formula in 5 minutes, clinicians quickly saw that her spleen was massive, and her platelet counts were rock bottom. Her liver was expanding—in a few months it looked like she had a volleyball in her stomach. These are the classic signs of Gaucher’s, a rare, recessive genetic disorder in which the body does not produce enough of a lysosomal enzyme that breaks down the fatty substance glucocerebroside, causing it to glob up in cells of the liver, spleen, and other organs—including, sometimes, the brain. But researchers have never seen the combination of mutations Hannah carries, so doctors couldn’t determine if she had the Type 2 or Type 3 form. Children with Type 2 typically die before their third birthdays, while those with Type 3 can live much longer. “They [wouldn’t] give us a prognosis,” Hannah’s mom, Carrie Ostrea, says. “They came out and said that to us. Which is fine by me.” © 1986-2010 The Scientist
Related chapters from BP6e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 13737 - Posted: 06.24.2010
By M. A. Woodbury President Franklin D. Roosevelt admonished in a 1932 commencement address that “it is common sense to take a method and try it. If it fails, admit it frankly and try another.” FDR had the revival of a depressed U.S. economy in mind, but scientists experimenting with treating brain disorders with fetal cell transplants have taken his aphorism to heart. New methods are transforming past failures, and the results seem far more promising this go-round. Fetal cell therapy began in earnest in the mid-1980s, among researchers hoping to treat Parkinson’s disease. These patients have trouble controlling their movements partly because their brains lack the neurotransmitter dopamine. The hope was that tissue from fetal midbrains placed into patients’ brains would turn into dopamine-making cells. Shortly after the turn of the century, however, the work foundered when a subset of transplant patients developed disabling movement disorders termed runaway dyskinesias. But amid the setbacks was the fact that some subjects—especially those who were younger and less afflicted—did well with the fetal cells. “The question is, How do we reconcile all these disparate strands and problems with these trials and move the field forward?” says Roger Barker, a neurologist at the University of Cambridge who is meta-analyzing prior transplant data in hopes of devising a better trial. One possible explanation for the mixed findings is contamination: transplant tissue containing serotonin-secreting neurons could have muddied the results. © 2010 Scientific American,
Related chapters from BP6e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 13665 - Posted: 06.24.2010
By Laura Sanders CHICAGO — A toned, buff bod isn’t the only thing a workout is good for. Exercise protects special brain cells in monkeys’ brains and improves motor function, a new study finds. The data, presented at a news briefing October 18 in Chicago at the Society for Neuroscience’s annual meeting, adds to a growing body of evidence that shows exercise is good for the brain, too. “This is sort of a quiet revolution that’s been occurring in neuroscience,” says Carl Cotman, a brain aging expert at the University of California, Irvine, “to realize that physical activity at a certain level impacts the brain in a really profound way.” In the new study, researchers led by Judy Cameron of the University of Pittsburgh trained six adult female rhesus monkeys to run on treadmills built for humans. Over a period of three months, monkeys either ran, jogged or sat on a treadmill for five hours each week. Monkeys that ran got their heart rates to about 80 percent of maximum, comparable to a human training program that would increase cardiovascular fitness. The jogging monkeys’ heart rates reached about 60 percent of maximum. After this training period, the researchers hit the right side of the monkeys’ brains with a neurotoxin called MPTP, designed to selectively kill neurons that produce the signaling chemical dopamine. These neurons, and the dopamine they produce, regulate movement, and are the very same ones that die in people with Parkinson’s disease. © Society for Science & the Public 2000 - 2009
By Larry Greenemeier Huber, Purdue, Moran, Parkinson'sParkinson's disease sufferers typically face a long, difficult battle against the disorder's degenerative effects on their motor skills and speech. While many scientists are studying the potential for drugs, surgery and exercise to slow the disease's impact on the central nervous system—including tremors, stiff muscles and impaired movement—one team of researchers is experimenting with technology designed to help Parkinson's sufferers fend off voice and speech problems. Parkinson's can leave its victims afflicted with speech that tends to be soft, hoarse and monotonous, particularly during the disease's later stages. Jessica Huber, an associate professor of speech, language and hearing sciences at Purdue University in West Lafayette, Ind., is in the early stages of developing a device that could help Parkinson's sufferers articulate their thoughts more audibly by exploiting the Lombard effect, a reflex in which people automatically speak louder in the presence of background sound (for example, at a sporting event, party or restaurant). Huber has created device that includes an earpiece that automatically plays ambient noise, mimicking the din of conversation typically found in a restaurant, whenever a person attempts to speak (this is detected by a sensor placed on the neck). A mask and sensors in elastic bands placed around the rib cage precisely record respiratory, laryngeal and articulatory data as the subject speaks. © 1996-2009 Scientific American Inc.
Related chapters from BP6e: Chapter 11: Motor Control and Plasticity; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 15: Language and Our Divided Brain
Link ID: 13210 - Posted: 06.24.2010
It may take a combination of three molecules to kill brain cells in Parkinson's disease, researchers say. The three molecules — the neurotransmitter dopamine, a calcium channel, and a protein called alpha-synuclein — act together, Eugene Mosharov of Columbia University Medical Center in New York and his colleagues said in Wednesday's online issue of the journal Neuron. "Though the interactions among the three molecules are complex, the flip side is that we now see that there are many options available to rescue the cells," Mosharov said in a release. Symptoms of Parkinson's include uncontrollable tremors and difficulty in moving arms and legs. Scientists had suspected that three molecules were involved in killing neurons. The new findings suggest how it may happen. Using a new electrochemical approach to growing neurons in the lab, the researchers were able to measure dopamine released outside the cells. It's the location of dopamine that matters. Dopamine outside the cells, known as cytosolic dopamine, is toxic to neurons, the researchers found. If dopamine is confined inside cells, it's safe. Neurons lacking alpha-synuclein were resistant to the toxic damage. © CBC 2009
By Laura Beil The patient, known as only “MBM,” was just 7 years old the first time doctors saw her. She had always been prone to night sweats, but now excessive perspiration was forcing her to change clothes several times a day. She was endlessly thirsty, fatigued and losing weight despite a voracious appetite. A dozen years later, at age 19, doctors checked her into a hospital, thinking she had some kind of unusual metabolic condition. After aggressive treatment with drugs, her symptoms improved, but only for a short time, and the next year surgeons removed most of her thyroid. When she was 35 — gaunt, weak and losing hair — doctors began searching every tissue of her body for a diagnosis. They finally located the problem. It was MBM’s mitochondria, the organelles that supply the energy for cells to function. Thanks to mitochondria, the sandwich you had for lunch is now powering your heart and brain. Somehow the mitochondria inside MBM’s cells had gone haywire, becoming too large and too numerous. Such damage was “the first instance of a spontaneous functional defect of the mitochondrial enzyme organization.” The mysterious case of patient MBM was considered so remarkable that the Journal of Clinical Investigation published a description of it. That was in 1962. Today, scientists suspect that millions of people may be suffering from mitochondria gone awry, in more subtle but nonetheless insidious forms. Evidence suggests that malfunctioning mitochondria could explain Alzheimer’s disease, Parkinson’s, diabetes, cardiovascular disease, obesity, cancer and other consequences of aging. © Society for Science & the Public 2000 - 2009
Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 12583 - Posted: 06.24.2010
By Nathan Seppa People who kick and lash out while fast asleep in bed face a high risk of developing Parkinson’s disease and certain forms of dementia, scientists report online December 24 in Neurology. The condition, called rapid-eye-movement sleep behavior disorder, results when a person’s muscles fail to relax during sleep. “During REM sleep, with the most vivid dreaming, mostly we’re paralyzed,” says neurologist Ronald Postuma of McGill University in Montreal. “The brain shuts off muscle tone. We want to run but we can’t.” But in people with REM sleep behavior disorder, muscle tone isn’t shut down. “As a consequence, you act out your dreams,” he says. People with the condition have been known to break a hand on a wall, hurt a spouse or fall out of bed, he says. Postuma and his colleagues have monitored the progress of 93 people who were diagnosed with REM sleep behavior disorder between 1989 and 2006 at Sacré Coeur Hospital, also in Montreal. The team followed some patients for 15 years or more. Roughly 80 percent are men, and most were enrolled while in their 60s. Of the 93 participants, 26 have developed a neurodegenerative disease during the study years. Of these, 14 developed Parkinson’s disease, and seven developed Lewy body dementia, which is marked by the appearance of Lewy bodies — abnormal protein deposits — in the brain. Four other study participants were diagnosed with Alzheimer’s disease, but the researchers suspect that these patients might actually have Lewy body dementia. One person developed a less common neurodegenerative condition called multiple system atrophy. © Society for Science & the Public 2000 - 2008
Related chapters from BP6e: Chapter 11: Motor Control and Plasticity; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 10: Biological Rhythms and Sleep
Link ID: 12380 - Posted: 06.24.2010
By Morten L. Kringelbach and Tipu Z. Aziz The video is brief, just a couple of minutes, but it’s reality TV as riveting as anything you’ll ever see. A man in his mid-50s, affable, articulate, faces the camera and talks a bit about a medical procedure he’s had. He holds in his hand what looks like a remote control. “I’ll turn myself off now,” he says mildly. The man presses a button on the controller, a beep sounds, and his right arm starts to shake, then to flap violently. It’s as if a biological hurricane has engulfed him, or perhaps it’s that his arm is made of straw and some evil sprite is waving it about. With effort, the man grasps the malfunctioning right arm with his left hand and slowly, firmly, subdues the commotion, as if he were calming a child in the throes of a temper tantrum. He’s breathing hard, and it’s clear he can’t keep it up much longer. With an almost desperate gesture, he reaches out for the controller and manages to press the button again. There’s a soft beep, and suddenly it’s over. He’s fine. Composed, violently afflicted, then composed again. All with the flick of a switch. As before-and-after moments go, this one is potent, verging on the miraculous. It’s the kind of thing you’d expect to witness under a revival tent, not in the neurology ward of a British hospital. Once you’ve seen it, you’ll have an indelible image of Parkinson’s disease. The word “tremor” doesn’t convey what can happen to people—the way they are thrashed and harassed by their own bodies. But this scene, involving a patient of ours, informs viewers about more than a disease; it’s a vivid window onto a powerful medical technology known as deep-brain stimulation (you can watch the video at www.kringelbach.dk/nrn). © 1996-2008 Scientific American Inc.
Related chapters from BP6e: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 12322 - Posted: 06.24.2010
By SANDRA BLAKESLEE Dr. Patrick J. Kelly, the head of neurosurgery at New York University, folded his arms hard against his chest, radiating skepticism. “I have a neurological problem that I’ve never told anyone about — not a soul,” he recalls saying to his colleague Dr. Rodolfo Llinás before an auditorium packed with neurosurgeons. “You listen to my brain and tell me what it is. If you do, I will believe you.” So it was that Dr. Kelly allowed his brain to be scanned in a MEG machine, a device that measures tiny magnetic signals reflecting changes in brain rhythms. After analyzing his colleague’s brain activity, Dr. Llinás announced: “You have tinnitus. Right brain. The phantom sound ringing in your ears must be very loud. It is low frequency, a rumbling noise.” Dr. Kelly was stunned, he said later. He had been hearing that noise ever since he served at a station hospital in Danang during the Vietnam War. The roar of helicopters dropping off casualties had permanently warped his hearing. Dr. Llinás, the chairman of neuroscience and physiology at the N.Y.U. School of Medicine, believes that abnormal brain rhythms help account for a variety of serious disorders, including Parkinson’s disease, schizophrenia, tinnitus and depression. His theory may explain why the technique called deep brain stimulation — implanting electrodes into particular regions of the brain — often alleviates the symptoms of movement disorders like Parkinson’s. Copyright 2008 The New York Times Company
By ABIGAIL ZUGER, M.D. Doctors get seriously ill just like ordinary people, and some of them never recover from the shock. If of a literary bent, they are often moved to reflect for posterity on this disruption of the natural order, detailing their former hubris and the enlightening misery of health care experienced from the other side of the bed. Against this generally lackluster collection of memoirs, Dr. Thomas Graboys’s stands out as a small wonder. Unsentimental and unpretentious, it manages to hit all its marks effortlessly, creating a version of the old fable as touching, educational and inspiring as if it had never been told before. The story’s success lies partly in its almost mythic dimensions: Dr. Graboys rose high, and he fell hard. Until age 50 he was a medical version of one of Tom Wolfe’s masters of the universe: a noted Harvard cardiologist beloved by colleagues and patients, happily married to a tall, beautiful blonde. He was a marathon runner, a demon on the tennis courts and ski slopes, and, if he says so himself, a particularly handsome guy. Then everything fell apart. Over a terrible two-year period Dr. Graboys’s wife died a lingering death from colon cancer. In his grief he barely noticed that he was not functioning quite as well as usual. Those around him figured his fatigue and uncharacteristic fumbling were only to be expected. He pulled himself together, met another woman, and then collapsed on the wedding day — the beginning of physical problems that could no longer be ignored. It was Parkinson’s disease, the neurological condition that makes the body stiffen and shake, but it took Dr. Graboys many months to take the irrevocable step of giving his problems a name. Copyright 2008 The New York Times Company
By Nikhil Swaminathan A successful treatment for Parkinson's disease, a neurodegenerative disorder that affects 1 percent of the world's population and (an estimated 500,000 people in the U.S.) aged 60 years and over, may be "in our sights now," says Ronald McKay, a researcher at the National Institutes of Health (NIH). McKay's optimism stems from new research that shows that a gene, known as forkhead box A2 (FOXA2), is responsible for the differentiation and spontaneous destruction of neurons that secrete the neurotransmitter dopamine, a cell population that is progressively lost in Parkinson's disease, which is characterized by tremors, loss of muscle control and speech difficulties. "We have the cells; we know what controls their birth and death—we're on our way," says McKay, a senior molecular biology investigator. "It looks like we've got this disease in our sights now. We will understand Parkinson's disease relatively soon." McKay and colleagues (at the NIH's National Institute of Neurological Disorders and Stroke in Bethesda, Md., and at Northwestern University's Feinberg School of Medicine in Chicago) report in the journal PLoS Biology that they tested candidate cells in the brain of embryonic mice to determine which ones produce the enzyme tyrosine hydroxylase, a compound manufactured by dopamine neurons to help convert amino acids into precursors of the neurotransmitter. © 1996-2007 Scientific American Inc.